A complex interplay
The notion of differentiation between Type 2 and non-Type 2 molecular phenotypes has been contested.
This is borne out by a study conducted by Seys S, et al (2017)5 which identified 5 unique asthma molecular phenotypes by biological clustering and found that Type 2 cytokines clustered with non-Type 2 cytokines in 4 out of 5 clusters. Their research points towards significant heterogeneity among asthmatic patients with Type 2 inflammation.
Defining Type 2 asthma, therefore, is a subject of intense investigation as it encompasses a wide range of endotypes and subendotypes.1,6 Consequently, the global prevalence of Type 2 versus non-Type 2 asthma is an area of ongoing research.
Prevalence of Type 2 Asthma
Over the past 20 years, studies have shown discrepancies around the exact prevalence of asthma in patients worldwide, ranging from 7% in France and Germany, 11% in the US and 15–18% in the UK.7 Due to the difficulty in predicting prevalence rates, there is also contention within Type 2 and non-Type 2 cluster phenotypes.
Type 2 asthma is further characterised by varying levels of ‘Th2 driven inflammation’ — ‘Th2-high’ and ‘Th2-low’ endotypes – with the former being diagnosed in roughly 50% of the mildly asthmatic population.1
However, while the prevalence of both Th2-high and Th2-low asthma has historically been considered to be the most commonly observed form within the asthma patient population, this notion has been challenged in more recent literature.
Type 2 asthma is a complex heterogeneous disease that encompasses a range of phenotypes and biomarkers8,9
As research is uncovering the heterogeneity within each class of asthma, more is being understood about this complex disease, with focus on how the cytokine milieu in the lung plays a critical role in the development and pathogenicity of Type 2 asthma, and how it contributes to disease severity.